Lung CSC‐derived exosomal miR‐210‐3p contributes to a pro‐metastatic phenotype in lung cancer by targeting FGFRL1
Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types...
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| Published in | Journal of cellular and molecular medicine Vol. 24; no. 11; pp. 6324 - 6339 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.06.2020
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1582-1838 1582-4934 1582-4934 |
| DOI | 10.1111/jcmm.15274 |
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| Abstract | Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types of cells that mediate cell interactions, including cancer metastasis. Here, we show that lung CSC‐derived exosomes promote the migration and invasion of lung cancer cells, up‐regulate expression levels of N‐cadherin, vimentin, MMP‐9 and MMP‐1, and down‐regulate E‐cadherin expression. Moreover, we verified that these exosomes contribute to a pro‐metastatic phenotype in lung cancer cells via miR‐210‐3p transfer. The results of bioinformatics analysis and dual‐luciferase reporter assays further indicated that miR‐210‐3p may bind to fibroblast growth factor receptor‐like 1 (FGFRL1); silencing FGFRL1 enhanced the metastatic ability of lung cancer cells, whereas overexpressing FGFRL1 suppressed metastasis. Taken together, our results provide new insights into a potential molecular mechanism whereby lung CSC‐derived exosomal miR‐210‐3p targets FGFRL1 to promote lung cancer metastasis. FGFRL1 may be a promising therapeutic target in lung cancer. |
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| AbstractList | Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types of cells that mediate cell interactions, including cancer metastasis. Here, we show that lung CSC‐derived exosomes promote the migration and invasion of lung cancer cells, up‐regulate expression levels of N‐cadherin, vimentin, MMP‐9 and MMP‐1, and down‐regulate E‐cadherin expression. Moreover, we verified that these exosomes contribute to a pro‐metastatic phenotype in lung cancer cells via miR‐210‐3p transfer. The results of bioinformatics analysis and dual‐luciferase reporter assays further indicated that miR‐210‐3p may bind to fibroblast growth factor receptor‐like 1 (FGFRL1); silencing FGFRL1 enhanced the metastatic ability of lung cancer cells, whereas overexpressing FGFRL1 suppressed metastasis. Taken together, our results provide new insights into a potential molecular mechanism whereby lung CSC‐derived exosomal miR‐210‐3p targets FGFRL1 to promote lung cancer metastasis. FGFRL1 may be a promising therapeutic target in lung cancer. Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types of cells that mediate cell interactions, including cancer metastasis. Here, we show that lung CSC-derived exosomes promote the migration and invasion of lung cancer cells, up-regulate expression levels of N-cadherin, vimentin, MMP-9 and MMP-1, and down-regulate E-cadherin expression. Moreover, we verified that these exosomes contribute to a pro-metastatic phenotype in lung cancer cells via miR-210-3p transfer. The results of bioinformatics analysis and dual-luciferase reporter assays further indicated that miR-210-3p may bind to fibroblast growth factor receptor-like 1 (FGFRL1); silencing FGFRL1 enhanced the metastatic ability of lung cancer cells, whereas overexpressing FGFRL1 suppressed metastasis. Taken together, our results provide new insights into a potential molecular mechanism whereby lung CSC-derived exosomal miR-210-3p targets FGFRL1 to promote lung cancer metastasis. FGFRL1 may be a promising therapeutic target in lung cancer.Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types of cells that mediate cell interactions, including cancer metastasis. Here, we show that lung CSC-derived exosomes promote the migration and invasion of lung cancer cells, up-regulate expression levels of N-cadherin, vimentin, MMP-9 and MMP-1, and down-regulate E-cadherin expression. Moreover, we verified that these exosomes contribute to a pro-metastatic phenotype in lung cancer cells via miR-210-3p transfer. The results of bioinformatics analysis and dual-luciferase reporter assays further indicated that miR-210-3p may bind to fibroblast growth factor receptor-like 1 (FGFRL1); silencing FGFRL1 enhanced the metastatic ability of lung cancer cells, whereas overexpressing FGFRL1 suppressed metastasis. Taken together, our results provide new insights into a potential molecular mechanism whereby lung CSC-derived exosomal miR-210-3p targets FGFRL1 to promote lung cancer metastasis. FGFRL1 may be a promising therapeutic target in lung cancer. |
| Author | Liu, Yanyang Wang, Li Hu, Haoyue Luo, Feng He, Jun Tu, Li Sun, Zhen |
| AuthorAffiliation | 2 Laboratory of Experimental Oncology State Key Laboratory of Biotherapy West China Hospital of Sichuan University Chengdu China 1 Lung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy West China Hospital of Sichuan University Chengdu China |
| AuthorAffiliation_xml | – name: 1 Lung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy West China Hospital of Sichuan University Chengdu China – name: 2 Laboratory of Experimental Oncology State Key Laboratory of Biotherapy West China Hospital of Sichuan University Chengdu China |
| Author_xml | – sequence: 1 givenname: Li orcidid: 0000-0002-9270-4544 surname: Wang fullname: Wang, Li organization: West China Hospital of Sichuan University – sequence: 2 givenname: Jun surname: He fullname: He, Jun organization: West China Hospital of Sichuan University – sequence: 3 givenname: Haoyue surname: Hu fullname: Hu, Haoyue organization: West China Hospital of Sichuan University – sequence: 4 givenname: Li surname: Tu fullname: Tu, Li organization: West China Hospital of Sichuan University – sequence: 5 givenname: Zhen orcidid: 0000-0003-3374-480X surname: Sun fullname: Sun, Zhen organization: West China Hospital of Sichuan University – sequence: 6 givenname: Yanyang surname: Liu fullname: Liu, Yanyang organization: West China Hospital of Sichuan University – sequence: 7 givenname: Feng surname: Luo fullname: Luo, Feng email: hxyyluofeng@sina.com organization: West China Hospital of Sichuan University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32396269$$D View this record in MEDLINE/PubMed |
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| Copyright | 2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| SubjectTerms | Antibodies Base Sequence Bioinformatics Biosynthesis Biotechnology Cell culture Cell interactions Cell Line, Tumor Endocytosis exosome Exosomes Exosomes - metabolism Exosomes - ultrastructure Fibroblast growth factors Gene Expression Regulation, Neoplastic Gene Silencing Genotype & phenotype Growth factors Humans Lung cancer lung cancer stem cell Lung Neoplasms - genetics Lung Neoplasms - pathology Membrane vesicles Metastases Metastasis MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR‐210‐3p Neoplastic Stem Cells - metabolism Original Phenotype Phenotypes Proteins Receptor, Fibroblast Growth Factor, Type 5 - metabolism Spheres Spheroids, Cellular - metabolism Spheroids, Cellular - pathology Stem cells Therapeutic applications Tumor microenvironment Tumors Vimentin |
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| Title | Lung CSC‐derived exosomal miR‐210‐3p contributes to a pro‐metastatic phenotype in lung cancer by targeting FGFRL1 |
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